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RC Test 1 > B4.017 Prework 3 Treatment of Cardiac Arrhythmias > Flashcards

B4.017 Prework 3 Treatment of Cardiac Arrhythmias Flashcards

1
Q

2 main classes of drugs used to treat arrhythmias

A

rate control agents

rhythm control agents

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2
Q

rate control agent classes

A

b-blockers (metoprolol, atenolol)
Ca2+ channel blockers (verapamil, diltiazem)
digoxin

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3
Q

rhythm control agents

A

Na+ channel blockers (Procainamide, quinidine, disopyramide, flecainide, propafenone)
K+ channel blockers (amiodarone, ibutilide, sotalol, dofetilide)

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4
Q

Class I overview

A

Na+ channel blockers
decrease HR by:
-elevating threshold for excitation
-decreasing slope of phase 4 depol in SA node

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5
Q

Class II overview

A

B blockers

-decrease HR

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6
Q

Class III overview

A

K+ channel blockers

-prolong AP duration and refractory period

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7
Q

Class IV overview

A

Ca2+ channel blockers

-decrease conduction velocity

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8
Q

Class IA overview

A

moderate Na+ channel block
dissociate with intermediate kinetics
prolong AP duration
also inhibit K+ channels

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9
Q

Class IB overview

A

mild Na+ channel block
fast dissociation
shorten AP duration
shortened repolarization

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10
Q

Class IC overview

A

strong Na+ channel block
slow dissociation
minimal effects on AP duration
no change in repolarization

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11
Q

members of Class IA

A

procainamide
quinidine
dispyramide

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12
Q

members of Class IB

A

lidocaine

mexiletine

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13
Q

members of class IC

A

flecainide
propafenone
moricizine

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14
Q

procainamide cardiac effects

A

increases effective refractory period of the atria and ventricles
can directly depress SA and AV nodes
prolongs AP duration by nonspecific blocking K+ channels

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15
Q

procainamide extracardiac effects

A

has ganglion blocking activity

reduced peripheral vascular resistance can lead to hypotension

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16
Q

procainamide toxicity

A

cardiotoxic: excessive AP prolongation, QT prolongation, induction of torsades de pointes, arrhythmia and syncope
long term: reversible lupus like syndrome (rash, arthralgia, arthritis, pericarditis)
other: nausea/diarrhea, rash, fever, hepatitis, agranulocytosis

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17
Q

procainamide therapeutic use

A

effective against most atrial and ventricular arrhythmias
short half life (3-4 hrs): oral dosing every 6 hours
less useful for long term (shoft half life and adverse effects)
2nd or 3rd choice for sustained ventricular arrhythmias associated w MI

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18
Q

quinidine cardiac effects

A

slows upstroke of action potential
slows conduction
QT prolongation due to K+ channel blocking
modest antimuscarinic effect

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19
Q

quinidine extracardiac effects

A

blocks a-adrenergic receptors to cause vasodilation

-hypotension and reflex tachycardia

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20
Q

quinidine toxicity

A 
increase plasma digoxin
precipitate digoxin toxicity
thrombocytopenia
syncope (due to torsades de pointes)
adverse GI effects (30-50%), cinchonism
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21
Q

quinidine therapeutic use

A

rarely used

better tolerated drugs available

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22
Q

disopyramide cardiac effects

A

similar to quinidine and procainamide but more antimuscarinic effects (tend to accelerate HR)

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23
Q

disopyramide toxicity

A

adverse effects caused by its pronounced atropine like activity

  • urinary retention
  • dry mouth, blurred vision, constipation
  • worsening of preexisting glaucoma
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24
Q

disopyramide therapeutic use

A

not used often bc of antimuscarinic effect
not first line bc negative inotropic action may induce CHF
ventricular arrhythmias only**

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25
Q

similarities between class IA antiarrhythmics

A

all block Na+, K+ channels, and can induce torsade de pointes

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26
Q

lidocaine administration

A

must be given IV

high first pass hepatic metabolism (only 3% in plasma)

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27
Q

lidocaine therapeutic use

A

ventricular arrhythmias associated with MI or digoxin toxicity
relatively ineffective in normally polarized tissues as in atrial flutter or fibrillation cardiac events

28
Q

lidocaine toxicity

A

low incidence of toxicity and high degree of effectiveness

29
Q

mexiletine administration

A

lidocaine analog, resistant to first pass hepatic effect so effective orally

30
Q

mexiletine uses

A

electrophysiologic and antiarrythmic actions like lidocaine
useful for ventricular arrhythmias
relief of chronic pain, esp diabetic neuropathy and nerve injury (off label)

31
Q

mexiletine adverse effects

A

predominantly neurologic

tremor, blurred vision, lethargy, nausea

32
Q

similarities of all Class IC drugs

A

all oral

increase mortality from cardiac arrest or arrhythmic rudden death in pts with recent MI

33
Q

flecainide mechanism

A

blocks Na+ and K+ channels, no QT prolongation

no antimuscarinic effects

34
Q

flecainide therapeutic use

A

supraventricular arrhythmias

very effective in suppressing premature ventricular contractions

35
Q

propafenone mechism

A

blocks Na+ channels

structurally similar to propranolol, thus weakly B blocking activity

36
Q

propafenone adverse effects

A

metallic taste

may exacerbate arrhythmias and cause constipation

37
Q

propafenone therapeutic use

A

supraventricular arrhythmias
very effective in suppressing premature ventricular contractions
(same as flecainide)

38
Q

moricizine mechanism

A

potent Na+ channel blocker that does not prolong action potential

39
Q

moricizine therapeutic uses

A

was used for ventricular arrhythmias

withdrawn from US market

40
Q

propranolol (nonselective) and atenolol (b1) therapeutic uses

A

rate control
supraventricular and ventricular arrhythmias caused by SYM stim
prevent v-fib

41
Q

esmolol (b1) therapeutic use

A

acute tachycardias occurring during surgery

42
Q

beneficial effects of b blockers

A

diminished SYM activation of heart and blood vessels

decreased cardiac workload

43
Q

harmful effects of b blockers

A

negative inotropy

may induce or worsen HF in patients w acute MI

44
Q

amiodarone therapeutic use

A

oral or IV
maintain normal sinus rhythm in patients with a-fib
prevent recurrent ventricular tachycardia

45
Q

amiodarone cardiac effects

A

prolongs AP duration (and QT interval) by blocking K+ channels
decreases rate of firing in pacemaker cells by blocking Na+ channels
blocks a and b adrenergic receptors and Ca2+ channels and this inhibits AV node conduction to produce bradycardia

46
Q

amiodarone extracardiac effects

A

peripheral vasodilation, esp after IV admin

47
Q

amiodarone toxicity

A

aymptomatic bradycardia and AV block in pts with AV/SA node disease
resp difficulties leading to fatal pulm fibrosis (1%)
abnormal liver function and hepatitis
skin deposits (grayish blue skin)
after a few weeks in essentially all pts: corneal microdeposits, reduced visual activity, optic neuritis, can progress to blindness
blocks thyroid function T4 to T3, can result in hyper or hypothyroidism

48
Q

amiodarone pharmacokinetics

A

long half life
rapid 3-10 days (50% of drug)
slow for several weeks> toxicity long after its discontinues

49
Q

amiodarone metabolism

A

CYP3A4

drug drug interactions

50
Q

dronedarone mechanism

A

structural analog of amiodarone without iodine

blocks several K+ and Na+ channels

51
Q

dronedarone adverse effects

A

no thyroid or pulm toxicity
liver toxicity
black box warning of increased death, stroke, a d heart failure in pts with decompensated heart failure and permanent a-fib

52
Q

sotalol mechanism

A

nonselective b adrenergic blocker that also prolongs AP duration and has antiarrhythmic properties
may cause prolonged repol resulting in torsade de pointes (6% at highest dose)

53
Q

sotalol therapeutic use

A

life threatening ventricular arrhythmias
maintaining sinus in a-fib
treatment of supraventricular and ventricular arrhythmias in pediatrics

54
Q

dofetilide (oral) and ibutilide (IV) mechanism

A

block rapid component of the delayed rectifier K+ current to slow cardiac repolarization

55
Q

dofetilide (oral) and ibutilide (IV) therapeutic use

A

restore normal sinus rhythm in a-fib or flutter

56
Q

dofetilide (oral) and ibutilide (IV) adverse effects

A

prolonged QT and torsade de pointes in 10% of pts

57
Q

verapamil and diltiazem mechanism

A 
orally active
block L type Ca channels in myocardium and vascular smooth muscle
depress SA/AV nodes directly to:
-decrease contractility
-reduce SA not automaticity
-slow AV node conduction
58
Q

verapamil and diltiazem therapeutic use

A

supraventricular arrhythmias

rate control in a-fib

59
Q

adenosine mechanism

A

opens inward rectifier K+ channels> hyperpolarization
inhibits L-type Ca channels > inhibits Ca entry and conduction CV in AV node
inhibits pacemaker current > decreases HR
mainly affects AV > SA

60
Q

adenosine therapeutic uses

A

IV injection
converts paroxysmal supraventricular tachycardia to sinus
highly efficient (90-95%)
very short half life

61
Q

adenosine adverse effects

A 
flushing
SOB
chest burning
headache
hypotension
nausea
paresthesia
62
Q

digoxin mechanism

A

potent and selective inhibitor of NA+/K+ ATPase > increased Ca2+ > positive inotrope
stimulated vagus nerve and thus decreases HR

63
Q

digoxin therapeutic use

A

can be used in a-fib to decrease rate
narrow window
other antiarrhythmic drugs enhance toxicity
many antibiotics increase digoxin absorption
drugs that produce hypokalemia will enhance toxicity (K+ is a competitor)

64
Q

digoxin toxicity

A

GI: nausea, vomiting, diarrhea, ab discomfort
cardiac: almost all arrhythmias

65
Q

magnesium therapeutic use

A

mag chloride or sulfate (parenteral)
mechanism unknown
prevent torsade de pointes
used against digoxin induced arrhythmias

RC Test 1 (19 decks)

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